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Maine Board of Pesticides Control

Miscellaneous Pesticides Articles

July 2015

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Some Maine retailers phasing out products that harm bees

By Eric Russell Portland Press Herald [email protected] | @PPHEricRussell | 207-791-6344

A growing number of Maine retailers have begun phasing out use of a class of pesticides that research shows harms honey bees, butconsumers may still be confused about what stores have done to get rid of them.

Neonicotinoids have come under closer scrutiny because of their effect on bees, which are vital to plant pollination, but the EnvironmentalProtection Agency still hasn’t taken a firm stance on banning production. Retailers, in part because of public pressure, are attempting toaddress the problem pesticides themselves, but there is no uniform policy. Some stores have pulled products with neonicotinoids fromshelves, some have begun labeling them and some have done nothing, creating confusion among consumers about which plants topurchase.

Pam Jones of Kennebunk holds a heather plant on Tuesday that she bought at Home Depot in Biddeford recently. Because the label onthe pot didn’t list any pesticides, Jones thought she was buying a pesticide-free heather plant. When she pulled the plant out of the pot toput it into the ground, she was surprised to find a label at the bottom of the pot stating the plant was treated with a pesticide containingneonicotinoids. She thinks plants that contain pesticides should be clearly labeled in an easy to see place. Portland Press Herald photo byGregory Rec

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Pam Jones of Kennebunk holds a heather plant on Tuesday that she bought at Home Depot in Biddeford recently. Because the label onthe pot didn’t list any pesticides, Jones thought she was buying a pesticide-free heather plant. When she pulled the plant out of the pot toput it into the ground, she was surprised to find a label at the bottom of the pot stating the plant was treated with a pesticide containingneonicotinoids. She thinks plants that contain pesticides should be clearly labeled in an easy to see place. Portland Press Herald photo byGregory RecSearch photos available for purchase:

Pam Jones, who lives in Kennebunk, found that out the hard way.

She uses organic soil in her garden and tries to avoid pesticides. When she purchased a heather plant recently from the Home Depot inBiddeford, she assumed it was free of neonicotinoid pesticide because there was no label on the plant indicating its presence.

It wasn’t until Jones got home and took the plant out of its temporary pot that she saw the label — stuck to the bottom of the plant.

“If that’s where they are putting these labels, what’s the point?” she said. “When I went back to the store, the clerk said several othercustomers had asked about labeling as well.”

Matt Harrigan, spokesman for Atlanta-based Home Depot, which has more than 2,200 stores worldwide, said the company — withguidance from the EPA — is still monitoring research on the effects of neonicotinoids on honey bees.

“In the meantime, we’re one of the few retailers that has started requiring our suppliers to label neonic-treated plants so customers whobelieve neonics are impacting the bee population won’t purchase those plants unknowingly,” Harrigan said in a statement. “The fact is,most nurseries sell at least some plants treated with neonics.”

Harrigan said all plants sold at Home Depot are supposed to be clearly labeled, but he couldn’t speak for every store.

Lowe’s, the second-largest home improvement chain, announced last year that it was phasing out the sale of all products that containneonicotinoid pesticides within 48 months. However, products that still contain neonicotinoids may not all be labeled.

“We are currently working with growers and suppliers of live plants to eliminate the use of neonic pesticides on bee-attractive plants we selland encouraging them to use biological pest control methods,” said Steve Salazar, manager of corporate communications for Lowe’s,based in North Carolina. “We plan to have plants and nursery products tagged with information highlighting bee health and encouragingcustomers to be mindful of pollinator health when using pesticides. The timeframe for adding the tags is being determined.”

Two southern Maine retailers, Eldredge Lumber and Hardware in York and Kittery Ace Hardware, have already removed several lawn andgarden products that contain neonicotinoids. The stores also have stopped carrying the widely used weed killer Roundup and isconsidering discontinuing other products that may have adverse environmental impacts.

“It is easy to order the stuff into the store, but almost impossible to return it to the manufacturers,” said owner Scott Eldredge. “Sure, I mightlose some sales, but I don’t care. There are potentially less harmful alternatives, and my staff is ready to help the public make better, saferchoices.”


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Eldredge said he hopes to eventually make his stores completely chemical-free.

Katherine Paul, associate director of the Organic Consumers Association and a Freeport resident, said many more retailers nationwidehave taken steps to eliminate the pesticides, although all have different timelines and guidelines for labeling.

Some other retail chains have yet to update their policies on neonicotinoids, she said, but are facing growing pressure.

The movement away from neonicotinoids is in part a response to a study published by Environmental Science and Pollution Research thatfound that pesticides were a key contributing factor in the population decline of honey bees.

The Environmental Protection Agency last month issued a moratorium that restricts the use of new pesticides, but the policy does notapply to products currently on the market.

“Unfortunately, the EPA, in deference to large pesticide-makers, is slow to move on regulating toxins like neonicotinoids,” Paul said. “Theshift away from toxic pesticides shows the power of consumer pressure on corporations to do the right thing.”

Staff Writer Eric Russell — 791-6344

Twitter: @PPHEricRussell

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Turf wars: Health debate accompanies Portland-areaartificial fields

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William HallTuesday, May 12, 2015 at 8:50 am

PORTLAND — Walking by the shuttered stands of Fitzpatrick Stadium, where finaltouches are now being made on a new artificial turf field, you might believe the adage: Thegrass really does grow greener on the other side of the fence.

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Photo: Ben McCanna / For The Forecaster

Caleb Johnson, a subcontractor of Northeast Turf of South Portland, smoothesfreshly laid artificial turf at Fitzpatrick Stadium in Portland on Thursday, May7.

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Photo: William Hall / For The Forecaster

"Crumb rubber," like the pellets seen here at a Yarmouth High School field andused as infill in other area artificial-turf playing grounds, may be linked tocancer, some health experts warn.

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Tony Johnson, an employee of Georgia-based Sprinturf, puts the finishingtouches on the soccer lines at the Yarmouth High School turf field two yearsago.

Photo: File

Construction of an artificial turf field at the Edward J. McMann OutdoorAthletic Complex at Morse High School in Bath in the summer of 2013.

Photo: File

Employees of Sports Turf International, a Scarborough company, install theturf playing field at Scarborough High School in 2006.

But some critics think recent alleged health concerns and questions about turf costs makeplaying grounds like Fitzpatrick, scheduled to re-open in less than a month, merely a fieldof dreams.

In October, NBC News aired a report about Amy Griffin, a women's soccer coach at theUniversity of Washington, who had noticed a disturbing trend. Beginning in 2009, Griffinhas compiled a list of 38 soccer players struck with cancer.

All 38 had played on artificial turf, and 34 of them were goalies, who are constantly divinginto the stuff.

"I've coached for 26, 27 years," she told NBC. "My first 15 years, I never heard anythingabout this. All of a sudden it seems to be a stream of kids (getting sick)."

Neither Griffin nor NBC claimed there was a causal link between the turf and cancer. Butthe coincidence has been enough to fuel a simmering debate about the safety of crumbrubber, the tiny pellets of recycled car tires used as "infill" cushioning in nearly all of thecountry's 11,000 artificial fields.

The rubber's composition is hard to pinpoint, but often includes toxic chemicals such aslead, other heavy metals and carbon black. Many of these are cancer-causing, and can beespecially dangerous to children and teens, whose bodies are still developing.

Nevertheless, Portland has gone ahead with plans to spend $835,000 to replace the artificialturf and surrounding running track at 6,000-seat Fitzpatrick.

The new field, including dark-blue end zones and emblazoned with a Portland High Schoolbulldog logo, is expected to open by June 20 for the state lacrosse championship and to behosting football and soccer this fall, according to Ethan Owens, the city's recreation andathletic facilities manager.

Nine of the 17 high schools in The Forecaster's coverage area now send their athletes toplay on artificial turf fields. Two of those – Fitzpatrick and the Yarmouth High Schoolvarsity field – are replacements for man-made grass installed in 2001. At that time, the twowere among the first artificial-turf playing surfaces in the state.

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Since then, turf-adopters have included Cape Elizabeth, Deering, Falmouth, Morse andScarborough high schools, as well as The Hyde School in Bath and North YarmouthAcademy.

And as at Fitzpatrick, Portland may double down by replacing the artificial turf at Deering'sMemorial Field in 2017, according to a city memo.

But opinion is divided about the fake fields.

Crumbs of evidence

School Administrative District 51 is now considering plans for a $1.6 million turf field atGreely High School in Cumberland. Yet the proposal has been under review for six monthsand it's not clear when or if a decision will be made, according to Eliza Miller, chairwomanof the district's Athletic Advisory Board.

Regional School Unit 5 in 2013 rejected a similar proposal at Freeport High School. So didSouth Portland in 2010. Morse built its $580,000 artificial-turf field in 2013, but only afterthe Bath City Council overcame three years of opposition, including a public referendumthat repealed an earlier approval.

While most local opposition has focused on the high up-front costs of installing artificialturf, concern about the health effects of crumb rubber has prompted other regions toreconsider their use of turf.

Kennedy Catholic High School in suburban Seattle decided not to use crumb-rubber infillafter the school principal viewed the NBC report. Last month, voters in Concord,Massachusetts, nearly passed a proposed two-year moratorium on the town's use ofartificial turf.

The Los Angeles Unified School District and the New York City Parks Department bothstopped construction of new fields with crumb rubber several years ago. The Californialegislature is now considering banning the use of state funds for such fields. And somemunicipalities have required chemical testing of their artificial-turf fields before players setfoot on them.

Owens isn't worried, however.

"It's pretty clear that there are really no issues," he said in a recent interview. "I kind of findit odd that we keep hearing these reports, when it's out there pretty explicitly that therereally are no troubles with the rubber."

He said the city's request for the turf replacement took a year to draft, and required the fieldto meet high industry standards for safety factors such as shock absorbency.

(Three turf companies submitted bids on the project; the winning bidder, Northeast Turf ofSouth Portland, also installed the stadium's first artificial surface.)

But there was no standard set for chemical safety and no requirement for study or testing.

"I don't think we did (testing) because of the information that is out there already," Owenssaid. "I think we felt there was no need because we would rely on the (industry) standardsand the ... studies that had previously been done."

Yarmouth's athletic director, Susan Robbins, shares Owens' confidence in the safety ofartificial turf. She called the NBC report "sensationalized."

"There's absolutely no link (to cancer)," she said recently. "As a parent here, I would neverput my own children at risk if I thought there was."

Like Owens, she cited scientific studies touting the safety of artificial turf. Fact sheetspublished by the turf industry cite dozens of them.

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But some health experts claim the studies are too limited to be useful, examining only asmall number of fields and the effects of only a small number of chemicals.

And regardless of the scientific debate, these experts say, there has been no study of turf'slong-term effects, simply because today's fields haven't been around very long.

In the beginning, AstroTurf

Artificial turf dates to 1966, when the first brand, AstroTurf – basically, short-pile nyloncarpeting laid over concrete – was installed at the Houston Astros' indoor baseball stadium.But crumb rubber infill has been used less than 20 years.

Reflecting the uncertainty, both the federal Environmental Protection Agency and theConsumer Product Safety Commission have recently back-pedaled from claims they mademore than five years ago that artificial turf is safe.

The EPA's website now states that it "is not possible to extend the results beyond the four(artificial fields studied) or to reach any more comprehensive conclusions without theconsideration of additional data."

And a CPSC spokesman last month told an Atlanta reporter that "what was done in 2008was not good enough to make a claim either way as to the safety of those fields.”

Local sports experts are keeping a close watch on the potential cancer risks of turf.

"There certainly seems to be some sort of a connection. Maybe it's worth a second look, tocontinue the research," said Matt Gerken, head athletic trainer at the University of Southern Maine, which installed turf in 2011. "But where do you draw the line?

"For now, we will continue to watch (the health risks) until we start to feel it's a problem. Ithasn't risen to that level yet."

Gerken, who served as trainer to the USM women's soccer team for 15 years, speculatedwhether crumb rubber infill could be inhaled, ingested or ground into an open cut orabrasion.

"Those rubber pellets get everywhere, cleats, coolers, socks," he said. "Those thingsmigrate."

At SAD 51, Miller said, "We've looked at the reports, and are investigating options forinfill" on the proposed Greely field. School Board members and Cumberland residents havealready asked questions about artificial turf's safety, she said.

Back at Fitzpatrick, Owens doesn't dismiss the cancer claims entirely.

"Like any product, you can buy the Yugo or you can buy the Cadillac," he said."Companies that make the Cadillac (turf) put in their time, they do the research, they makesure the rubber they use is a clean rubber. The others? Well, who knows where their rubbercomes from?"

Artificial turf provides a more uniform playing surface that is easier on athletes' joints, headds. And the high price tag of the turf is offset by maintenance that is far less costly than anatural grass field's.

Still, municipalities such as Montgomery County, Maryland, estimate that the need toreplace turf every eight years or so makes the long-term costs of both field types about thesame.

Owens believes the bigger advantage is the heavy use turf can take. Fitzpatrick could onlyaccommodate about 140 hours of use annually when the field was grass; in its last seasonof use, the turf field hosted 3,500 hours of play.

"If I was going to have this as a grass field, there would be a night and day difference," he

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said. "You'd only have varsity teams out there. You wouldn't have community use."

Last week, as workers prepared to lay down the first rolls of new turf, a visitor wonderedwhen the project would be finished.

"It can't be soon enough," said Patricia Allen, whose children attended Portland schools andwho often walks the track. "I worry a bit when I think about those rubber bits and what theycould do. But I guess that's a risk we have to take."

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Buffer zones are required around fields treated with some pesticides, including chlorpyrifos, which has been linked to neurological effects in children.

The EPA is on the clock to decide the future of a popular pesticide linked to health problems

June 11, 2015

By Brian Bienkowski (../../../../archives.jsp?sm=ts63%3B1title%2Clede%2Cdescription%2Csubject%2Cpublishername%2Ccoverage%2Creporter18%3B%22Brian+Bienkowski%22)Environmental Health News

A California appeals court ruled this week that the U.S. Environmental Protection Agency has until the end of this month to decide whether or notto ban a widely used pesticide linked to a number of health problems.

The order, filed yesterday by the 9th Circuit Court of Appeals, forces the EPA’s hand on the pesticide chlorpyrifos (pronounced KLOR – pie -ra –phos), one the most commonly applied organophosphate pesticides with an estimated 10 million pounds applied annually.

While banned for more than a decade for household use, it’s still used commercially on corn, soybeans, fruit and nut trees and some golfcourses. In 2012 the EPA required homes and schools to have buffers to reduce exposure.

The order is in response to a lawsuit filed in 2007 by the Pesticide Action Network and the Natural Resources Defense Council calling for the EPAto cancel registration for the pesticide.

US EPA forced to decide this month on pesticide’s fate — Environmenta... http://www.environmentalhealthnews.org/ehs/news/2015/jun/us-epa-forc...

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While manufacturers such as Dow Agrosciences have maintained the safety and efficiency of chlorpyrifos, scientists have expressed concernover what it does to exposed people. Various studies have linked it to birth defects, low birth weights (http://www.ncbi.nlm.nih.gov/pubmed/15238288/) and impaired brain development (http://www.epa.gov/ncer/events/news/2010/04_05_10_feature.html), and endocrine disruption(http://www.ncbi.nlm.nih.gov/pubmed/9588346).

Fetuses exposed to the pesticide while in the womb are most at risk.

The EPA has until June 30 to respond to the lawsuit. [See yesterday's court order here.] (http://cdn.ca9.uscourts.gov/datastore/opinions/2015/06/10/14-72794.pdf)

“It is time for EPA to protect children in the face of overwhelming scientific evidence that this pesticide causes brain damage in children,” saidEarthjustice attorney Patti Goldman, who represented the groups in the lawsuit, in a statement. “EPA has dragged its feet for far too long in theface of harm to children and workers.”

An EPA report earlier this year found that chlorpyrifos poses health risks to workers who mix and apply it and also can contaminate drinkingwater.

“We are concerned about some workers who mix, load and apply chlorpyrifos to agricultural and other non-residential sites,” the EPA wrote aboutthe report. “We are also concerned about workers who work around areas that are treated with chlorpyrifos, even if they are not using chlorpyrifosproducts as part of their jobs.”

If EPA intends to deny the administrative petition, “the final denial shall be issued no later than September 15, 2015,” according to the court order.

EHN welcomes republication of our stories, but we require that publications include the author's name and Environmental Health News at the topof the piece, along with a link back to EHN's version.

For questions or feedback about this piece, contact Brian Bienkowski at [email protected] (mailto:[email protected]).

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By Alex Acquisto, The ForecasterPosted June 11, 2015, at 2:33 p.m.

SOUTH PORTLAND, Maine — Protect South Portland has set its sights on a new goal: eliminate the use of pesticides.City Council chambers were filled to maximum capacity by members of the grassroots group and others Monday night, manyof whom spoke during the public comment portion of the meeting.After three presentations on the dangers of using and being exposed to pesticides, and the availability of viable, organicalternatives, each councilor and every resident who spoke agreed that the use of chemicals on public and private propertyneeds to be curtailed.“The perfect lawn is not our goal. Our goal is the perfect life. It’s about living well,” Councilor Maxine Beecher said.Jay Feldman, executive director of Beyond Pesticides, a national coalition against the use of pesticides, was among thosewho presented information to the council.“A lot of the adverse effects we suffer from today are clearly linked to pesticide exposure, among other things,” Feldman said.“This is a critical issue in today’s world.“We believe you, as legislators, can adopt for this community incentives through law that will ensure that organic systemsare put in place at the same time that you meet community expectations,” he said.“The bottom line is, whether we all agree, the fact is that there are proven issues with some of these products, and we haveviable alternatives now that will work,” Chip Osborne of Osborne Organics in Marblehead, Massachusetts, said.Homeowners use “80 million pounds of toxic pesticides each year in pursuit of the perfect lawn,” he said.Transitioning from inorganic fertilizers and weed killers isn’t just about changing one’s habit, Osborne said, it’s aboutchanging the approach entirely.“It’s a system-based approach versus a product-based approach. It’s conceptually different. [Using organic methods] isproblem solving, not symptom treating,” he said. “We’re taking a feed-the-soil approach as opposed to feed the plant.”Mary Cerullo, associate director of Friends of Casco Bay, said the effects aren’t just seen on land, but in the water.“About 10 years ago, we started thinking, what’s the possible impact of pesticides and herbicides on Casco Bay?” Cerullo toldthe council.From 2001 to 2009, Friends of Casco Bay sampled stormwater runoff for pesticides as it flowed into Casco Bay. Theirfindings showed 13 coastal runoffs in southern Maine with detectable levels of pesticide.In the public comment portion of the workshop, Rick Towle, director of parks, recreation and waterfront for the city, saidthat while South Portland “complies with all federal, state and local guidelines, those may or may not be enough.”The city does not have a formal, integrated pest management program in place, Towle said, “but that doesn’t mean that thecity doesn’t use best practices or follow those guidelines.”

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In many ways, the city has been aware of this threat for a while, and other, very expensive precautions have been taken alongthe way, Councilor Claude Morgan said.“Because the eyes of the world may be upon us, there’s a certain kind of sexiness to this work, but I think it’s also veryimportant to remember that South Portland has been leading the way in the drudgery work for two decades,” Morgan said.“We have been consistently digging up our grounds and completing our combined system overflow system.”This project, Morgan said, “is all about preventing flow from getting into our bay.”Adopting an ordinance that would curb the use of pesticides in the city would be a “very simple” effort that the city canmake, “which really costs us nothing and it’s just a continuation of the slog work that we’ve been doing for decades,” he said.All councilors expressed a desire to see an ordinance tailored to South Portland’s needs proposed in a timely manner.“If not now, when? What more do we need to move in the right direction?” Councilor Patti Smith said.“I’m ready to move forward as quick as we can do it,” said Morgan, who requested that city staff draft an ordinance to beexamined by the council at a July workshop.Resident Meg Braley of Beech Street said it feels like “we’re riding a wave, and it’s a very exciting wave to be on. It’s a wave ofthe future. I love that we are considering this and educating ourselves.”Protect South Portland formed in 2013 to promote a citizen-initiated referendum that would have banned the flow of tarsands from Canada to South Portland through a pipeline operated by Portland Pipe Line Corp.Although that effort narrowly failed, the City Council eventually adopted a “Clear Skies Ordinance” backed by the group thatprohibits the bulk loading of crude oil, including tar sands, onto ships in the city.

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Spraying on track toward controversyBy Eric BlaisdellSTAFF WRITERMONTPELIER — After a one-year hiatus, the Vermont Rail System has a permit to spray herbicides nextmonth on the track that runs through Montpelier, much to the dismay of residents and officials in theCapital City.

Last year, the Vermont Pesticide Advisory Council, a division of the Agency of Agriculture Food andMarkets, declined to allow the railroad to spray herbicide on the track from Pioneer Street in Montpelier tothe Interstate 89 overpass. According to the minutes from the meeting in May 2014, several Montpelierresidents expressed concerns over herbicides being used on the track and the possible health impacts. Theresidents wanted the railroad to use alternatives to herbicide in its effort to keep the track clear and safefor travel.

When the idea of a one-year hiatus was brought up, spokesmen for the railroad said it was possible, as the2.5-mile section of track was sprayed in 2013, reducing the possibility of track degradation. The councilthen approved the hiatus, with the understanding that the railroad would work with the state and the publicover the year to find alternatives.

John Snell, chairman of the city’s Tree Board, volunteered to act as the public liaison for the conversationsabout alternatives. He said Monday those conversations never happened because the railroad never got intouch with him.

The railroad did not return a request for comment Monday.

At its meeting in April, the pesticide council again discussed spraying on the track in Montpelier. Accordingto the draft minutes, railroad spokesman Ben Delorme told the council that a “cooperative effort” could notbe achieved. When pressed by the council why the effort failed, Delorme said a suggested volunteer effortto remove weeds was not viable because of safety concerns for the volunteers working on the track. Hesaid the railroad would also have to fund the effort for equipment and materials.

The council then approved the railroad’s permit, which included spraying in Montpelier, and the permit wasissued in May stating the spraying would occur in July.

Snell said he doesn’t want the track to be unsafe. “But there have got to be viable alternatives to whatthey have been doing,” he said.

Snell said if the herbicide is used, those people who live or walk in the area will have their safety injeopardy.

Barbara Burnett lives on Barre Street about a block from the track. Burnett said Monday she is medicallysensitive to chemicals and would have to live somewhere else during spraying.

She called it appalling and outrageous that the railroad could ignore the council’s instructions aboutworking with the public for alternatives.

“(The railroad) can just not do what they were told to do and then do whatever they want,” she said.

Burnett said there are several vegetable gardens along the track in the city that would be hit with theherbicide. She said those who walk the bike path in the city also could be exposed to the chemicals.

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Mayor John Hollar said Monday he had been in contact with Agency of Agriculture Food and MarketsSecretary Chuck Ross about the issue. Hollar said the railroad is private property owned by the railroad andregulated by the state.

He said he doesn’t know enough about any possible alternatives to make a suggestion for one; and hedoesn’t know the extent of the health risks for the herbicide. As he understands it, the herbicide to be used— Glyphosate — and the quantities used are safe.

Hollar said he would be working with the state and the railroad to look into alternatives and to see whetherthere is anything the city can and should do about the issue.

Secretary Ross said Monday the railroad is bound by the federal government to make sure the rails areclear. He said herbicide spraying is nothing new and is done in many places. Even so, he’s hopeful thedifferent parties can sit down for a meeting soon in an effort to find an alternative to the herbicide.

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DDT Exposure in Utero and Breast Cancer

Barbara A. Cohn, Michele La Merrill, Nickilou Y. Krigbaum, Gregory Yeh,June-Soo Park, Lauren Zimmermann, and Piera M. Cirillo

Child Health and Development Studies (B.A.C., N.Y.K., L.Z., P.M.C.), Public Health Institute, Berkeley,California 94709; Department of Environmental Toxicology (M.L.M.), University of California, Davis,California 95616; Environmental Chemistry Laboratory (G.Y., J.-S.P.), California Department of ToxicSubstances Control, Berkeley, California 91311; and Public Health Institute (G.Y.), Oakland, California94607

Context: Currently no direct evidence links in utero dichlorodiphenyltrichloroethane (DDT) expo-sure to human breast cancer. However, in utero exposure to another xenoestrogen, diethylstil-bestrol, predicts an increased breast cancer risk. If this finding extends to DDT, it could havefar-reaching consequences. Many women were heavily exposed in utero during widespread DDTuse in the 1960s. They are now reaching the age of heightened breast cancer risk. DDT exposurepersists and use continues in Africa and Asia without clear knowledge of the consequences for thenext generation.

Hypothesis: In utero exposure to DDT is associated with an increased risk of breast cancer.

Design: This was a case-control study nested in a prospective 54-year follow-up of 9300 daughtersin the Child Health and Development Studies pregnancy cohort (n � 118 breast cancer cases,diagnosed by age 52 y and 354 controls matched on birth year).

Setting and Participants: Kaiser Foundation Health Plan members who received obstetric care inAlameda County, California, from 1959 to 1967, and their adult daughters participated in the study.

Main Outcome Measure: Daughters’ breast cancer diagnosed by age 52 years as of 2012 wasmeasured.

Results: Maternal o,p�-DDT predicted daughters’ breast cancer (odds ratio fourth quartile vs first �

3.7, 95% confidence interval 1.5–9.0). Mothers’ lipids, weight, race, age, and breast cancer historydid not explain the findings.

Conclusions: This prospective human study links measured DDT exposure in utero to risk of breastcancer. Experimental studies are essential to confirm results and discover causal mechanisms. Find-ings support classification of DDT as an endocrine disruptor, a predictor of breast cancer, and amarker of high risk.

Diethylstilbestrol (DES) is a synthetic estrogen, whichwas prescribed to pregnant women until it was

banned in the United States in 1971 and is a seminal ex-ample of a transplacental carcinogen (1). The discoverythat DES exposure in utero causes clear-cell carcinoma ofthe vagina and cervix (2) and also predicts higher risk forbreast cancer (3) raises the possibility that other man-

made chemicals, particularly those that disrupt normalestrogen-related functions, could cause breast cancer inlater life. Although DES (4) and other exogenous estro-genic chemicals (5, 6) have been shown to cause mammarycancer experimentally, no other in utero chemical expo-sures have been quantified and related prospectively to

ISSN Print 0021-972X ISSN Online 1945-7197Printed in USACopyright © 2015 by the Endocrine SocietyReceived April 2, 2015. Accepted June 1, 2015.

Abbreviations: CCR, California Cancer Registry; CERLab, Clinical and Epidemiologic Re-search Laboratory; CHDS, Child Health and Development Studies; CI, confidence interval;DDE, dichlorodiphenyldichloroethylene; DDT, dichlorodiphenyltrichloroethane; DDTs,DDT compounds such as the isomers p,p�-DDT and o,p�-DDT; DES, diethylstilbestrol; DMV,Department of Motor Vehicles; OR, odds ratio.

O R I G I N A L A R T I C L E

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risk of breast cancer in a human population. The presentstudy addresses this gap.

The influence of these in utero exposures in cancer riskinformed an Endocrine Society scientific statement em-phasizing that the timing of an exposure either to a hor-mone or an endocrine disruptor determines its effects (7).For this reason, human studies of adult exposure to es-trogenic chemicals in relation to breast cancer risk are notsufficient (8, 9). Indeed, prior studies that investigated theassociation between midlife exposure to the pesticide di-chlorodiphenyltrichloroethane (DDT) and breast cancerwere largely negative (10).

We reported the one prior prospective and quantitativestudy to consider the implications of young age at DDTexposure on breast cancer risk. This study was based onincident breast cancer diagnosed before age 50 years in themothers’ generation of the Child Health and DevelopmentStudies (CHDS) pregnancy cohort over a 17-year fol-low-up (11). We used age in 1945, when DDT was widelyintroduced into the United States as a proxy for earliest ageat DDT exposure to evaluate whether there was an in-creased susceptibility to breast cancer among women withearly life exposure to DDT. We found that mothers whowere exposed to DDT prior to age 14 years showed a5-fold increase in risk of breast cancer (66th percentile ofserum p,p�-DDT compared with the 33rd percentile); riskwas greatest for women who were exposed even earlier, byage 4 years, and the DDT association with breast cancerwas observed only for women who were exposed prior toage 14 years (P � .02 for interaction between p,p�-DDTand age in 1945). These findings clearly support the needto further investigate the role of early-life DDT exposurein later breast cancer risk. Other than this study, there isan absence of human breast cancer studies of in uteroexposure to the DDTs (DDT compounds such as the iso-mers p,p�-DDT and o,p�-DDT that are found in technicalDDT and also compounds that are breakdown products ofDDT such as p,p�-dichlorodiphenyldichloroethylene(DDE), the most prevalent and persistent metabolite ofp,p�-DDT) (12) due in part to the logistic barriers of quan-titative assessment of gestational exposure coupled withfollow-up of at least 50 years needed to identify breastcancer cases (13), given that the median age at diagnosis is61 years (14).

DDT remains relevant to living populations for numer-ous reasons. First, most women born while DDT was ex-tensively used worldwide are still alive today and are henceat risk for breast cancer. Second, DDT remains in activeuse for control of malaria in Africa and Asia in accordancewith World Health Organization recommendations de-spite intense debate (15, 16). Third, because of its persis-tent presence in the environment, people worldwide con-

tinue to be exposed to DDTs that are already present (17).Environmental contamination and human exposure aregreater where use was recent and where safer use, storage,and disposal are challenging (18), such as in China (19)and areas in Mexico (20, 21) and Africa (22, 23). Indeed,DDT health effects will remain relevant for the foreseeablefuture, given that the distribution of malaria vectors ispredicted to expand with climate change (24). Meltingglaciers release DDTs into arctic waters in which it isknown to bioaccumulate to 1 million-fold higher concen-trations in people, reaching levels found among popula-tions with endemic malaria in tropical regions in whichDDT use remains in effect (25, 26).

Here we conducted the first prospective study to relatequantitative measures of in utero DDT exposure to risk ofbreast cancer in daughters.

Materials and Methods

SubjectsThis unique study is made possible by a 54-year follow-up of

20 754 pregnancies, resulting in 9300 live-born female offspringin the CHDS pregnancy cohort.

The CHDS was designed to examine the association betweenprenatal exposures and health and development over the lifecourse for parents and children. The CHDS recruited womenresiding in the area of Oakland, California, who were membersof the Kaiser Foundation Health Plan and received obstetric carefor pregnancies between 1959 and 1967 (27). More than 98% ofall eligible women enrolled. CHDS founding mothers voluntarilyparticipated in an in-person interview and gave permission toresearchers for medical record access for themselves and theirchildren. Their blood specimens were collected at several timesthrough pregnancy and 1–3 days after delivery. The presentstudy was reviewed and approved by the Institutional ReviewBoard of the Public Health Institute (Oakland, California), andwe have complied with all federal guidelines governing use ofhuman subjects.

Breast cancer casesAll members of the CHDS cohort are linked to the California

Department of Motor Vehicles (DMV) files on a regular basis todetermine California residence history, allowing us to updateany name changes. All names registered with the DMV are usedin establishing a match. Simultaneous linkage of multiple familymembers enhances matching. The regular DMV matching pro-vides a history of location for each subject, which is used todetermine the population at risk for cancer, corresponding withgeographic surveillance by California’s cancer registries.

Breast cancer cases were identified by linkage to the Califor-nia Cancer Registry and the California Vital Status Records aspreviously described (11, 28) and by self-report during a surveyof CHDS daughters conducted from 2010 to 2013. All names foreach CHDS subject were submitted for cancer linkages usingfixed (ie, birth date, sex, race, and name) and changeable (ie,address and patient record number) identifiers. A rigorous pro-tocol was used to verify cases, comparing fixed vs changeable

2 Cohn et al In Utero DDT and Breast Cancer J Clin Endocrinol Metab


identifiers by manual review. The California Cancer Registry(CCR) is reported to be greater than 99% complete after a lagtime of about 2 years (29). We ascertained 80% (n � 94) of thecases via CCR linkage as of 2012 and 20% (n � 24) via self-report as of 2013. Due to the CCR lag time, the self-reportedcases are more recently diagnosed than those from CCR. Tumorcharacteristics were available for 87% of CCR cases and for 50%of self-reported cases. Thus, we expect to have more completeinformation on tumor pathology with continuing CCR linkage.

Cases were defined as CHDS daughters with incident invasiveor noninvasive breast cancer diagnosed by age 52 years, identi-fied through surveillance and through self-report through Marchof 2013. There were 137 cases who met this case definition,diagnosed as of 2012. To be included in the present study, caseswere required to have a maternal perinatal blood sample formeasurement of DDT exposure, resulting in inclusion of 118cases (86%). Three controls, matched on birth year and trimesterof maternal blood draw, were selected at random for each casefrom among those who were under cancer surveillance andknown to be free of breast cancer at the age of diagnosis for thematching case. Inclusion in the present study also required avail-able data for the following variables known to be correlated withDDT exposure and potentially daughters’ breast cancer: mater-nal lipids, age, race, early pregnancy weight, height, and historyof breast cancer and whether the daughter was breast-fed, re-sulting in a final sample size of 103 cases (87% of those withserum samples) and 315 controls (83% of those with serumsamples).

Serum assaysIn 2014, we measured DDTs and serum lipids in nonfasting

maternal perinatal serum samples that had been collected from1959 through 1967. The mean age of subjects when blood wasdrawn was 26.9 years. We preferred to use the early postpartumsamples (collected within 1–3 d after delivery) when available toconserve serum for future studies when timing within pregnancyis more critical. Early postpartum samples were available andused for most case-control strata (77.7%); third-trimester sam-ples were used for 17.7%; second-trimester samples were usedfor 3.8%; and first-trimester samples were used for 0.7%. Priorwork has established that organochlorine levels are consistentacross all trimesters of pregnancy and soon after delivery withinwomen (30). Serum samples had been stored at �20ºC and werefirst thawed to prepare an aliquot of 1.5 mL for organochlorineassays. Aliquots were then shipped frozen to the laboratory of theCalifornia Department of Toxic Substances Control where theywere assayed for DDTs, including p,p�-DDT and o,p�-DDT, theprimary constituents of technical DDT, and the primary metab-olite of p,p�-DDT, DDE using methods developed previously(31).

Briefly, human serum samples (1 mL) spiked with surrogatestandards (tetrachloro-m-xylene, polychlorinated biphenyls-14,-65, and -166) were denatured with formic acid, extracted usingOasis HLB SPE cartridges (Waters Corp) and subsequentlycleaned up with 33% sulfuric acid silica using an automatedsample extraction system (RapidTrace; Biotage). DDT com-pounds (o,p�-DDT, p,p�-DDT, and p,p�-DDE) were analyzed ona DB-5ms column (30 m � 0.25 mm inner diameter, 0.25 �mfilm thickness; Agilent Technologies) installed in an Agilent gaschromatograph-tandem mass spectrometer (7890/7000B se-ries). Chromatographic conditions included pulsed splitless in-

jection at 250°C and helium carrier gas at 1 mL/min. The gaschromatograph temperature program started with an initial tem-perature of 90°C, a hold for 1 minute, a ramp of 50°C/min to150°C, a hold for 1 minute, a ramp of 8°C/min to 225°C, a holdfor 6.5 minutes, and a final ramp of 14°C/min to 310°C, a holdfor 6 minutes. The mass spectrometer was operated in electronimpact ionization mode using multiple reaction monitoring,source temperature of 275°C, ionization energy of 70 eV, andmass resolution of 1.2 amu. A calibration curve, consisting of fiveto eight standards with concentrations ranging from 0.1 to 30pg/�L (DDTs) or from 0.1 to 800 pg/�L (DDE) and an R2 valueof 0.990 or greater, was used for quantitation.

Each batch of 10 samples was analyzed using a standard qual-ity assessment and control protocol: a laboratory method blank(HyClone bovine serum; Fisher Scientific), a matrix spike in bo-vine serum, and a standard reference material (1958; NationalInstitute of Standards and Technology). Matrix spike recoveriesfrom bovine serum for p,p�-DDE, p,p�-DDT, and o,p�-DDT con-geners ranged from 93% � 14%, 102% � 19%, and 101% �12%, respectively. Precisions from 51 standard reference mate-rial samples were reasonable, eg, coefficients of variation were12%, 19%, and 14% for p,p�-DDE, p,p�-DDT, and o,p�-DDT,respectively. The method detection limits, calculated as 3 timesthe SD of the concentrations in method blanks (n � 51), were0.013 ng/mL o,p�-DDT, 0.054 ng/mL p,p�-DDT and 0.158ng/mL p,p�-DDE. Sample order was randomly assigned withinand across batches. Case-control strata were analyzed in thesame batches to minimize differences due to laboratory drift. Thelaboratory was blind as to case or control status of the samples.Interbatch and intrabatch coefficients of variation were 15% and5% for p,p�-DDT, 6% and 5% for p,p�-DDE, and 11% and 7%for o,p�-DDT, respectively. The proficiency of the laboratory isdemonstrated through regular successful participation in theArctic Monitoring and Assessment Program (32) testing rounds(z-score � 1).

Using 150 �L undiluted serum, total cholesterol and triglyc-erides were measured enzymatically on a Roche P Modular sys-tem using reagents and calibrators from Roche Diagnostics at theClinical and Epidemiologic Research Laboratory (CERLab) atBoston Children’s Hospital, which is certified by the Centers forDisease Control and Prevention/National Heart, Lung, andBlood Institute Lipid Standardization Program. For cholesterolthe method combines the specificity of the enzymatic reactionwith peroxidase/phenol-4-aminophenazone indicator reaction(33). Cholesterol esters are hydrolyzed by cholesterol esterase toproduce free cholesterol. In the presence of oxygen and choles-terol oxidase, cholesterol is oxidized to cholest-4-en-3-one andH2O2. The latter product then reacts with a dye to generate aquinoneimine dye. The intensity of the generated color is mea-sured at 505 nm and is directly proportional to the concentrationof cholesterol in the measured sample. At cholesterol concentra-tions of 132.8 and 280.4 mg/dL, the day-to-day reproducibilityin the CERlab, reflected by coefficient of variation, is 1.7%(SD � 2.4 mg/dL) and 1.6%, respectively (n � 693).

Triglycerides were measured enzymatically with correctionfor endogenous glycerol (34). In a preliminary reaction, the en-dogenous glycerol is phosphorylated in the presence of glycerolkinase and ATP. The formed glycerol-3-phosphate is oxidized togenerate H2O2, which reacts with 4-chlorophenol to produce anoxidative product. Then in the actual assay reaction, triglycer-ides are hydrolyzed by lipase mixture to generate glycerol andfatty acids. Similarly to the preliminary reaction, glycerol is phos-

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phorylated by the action of glycerol kinase and the generatedglycerol-3-phosphate is oxidized to produce H2O2. The latterproduct reacts with a dye to generate a colored product. Theintensity of the generated color is measured at 505 nm and isdirectly proportional to the concentration of triglycerides in themeasured sample. Triglycerides at concentrations of 84.0 and201.8 mg/dL are determined in in the CERLab with a day-to-dayreproducibility of 1.8% (SD 1.6 mg/dL) and 1.7% (SD 3.5 mg/dL), respectively (n � 675).

Statistical analysisData analyses were performed using age-matched, condi-

tional logistic regression. Each DDT variable (o,p�-DDT, p,p�-DDT, and p,p�-DDE) was categorized in quartiles of the loggeddistribution based on the control population and represented asthree nominal variables in models: quartile 2, quartile 3, andquartile 4 in which quartile 1 was the reference category.

We used a likelihood ratio criterion (P � .05) to choose thebest model from among the following nested models: 1) all threeDDT compounds were entered into the model, 2) terms for oneof the three compounds was deleted beginning with the com-pound showing the highest P values and smallest effect sizes, and3) models with only one DDT compound included. Trendsacross quartiles of DDT compounds in the best model were testedusing natural log-transformed continuous variables. All modelswere adjusted for serum total cholesterol and total triglyceridesentered as natural logs, maternal age (continuous), race (AfricanAmerican vs non-African American), overweight in early preg-nancy (coded as overweight vs not, based on a body mass index �25 kg/m2), parity (primiparous vs multiparous), maternal his-tory of breast cancer (yes vs no), and whether the daughter wasbreast-fed. The final model deleted adjustment variables that hadlittle or no influence on the DDT predictors as evidenced by lessthan 10% change in the DDT coefficient(s) when removed fromthe model. Saturated interaction models were also tested for thethree DDT variables (coded as continuous log transformed vari-ables) and for the DDT variables in the final model with each

potential confounder. These were not significant and are notreported.

Results

Distributions of study variables are shown in Table 1.There were significant correlations among the DDT vari-ables. However, the correlation of o,p�-DDT with p,p�-DDT was higher (Spearman rank correlation coefficient0.78) than the correlation of either of these compoundswith p,p�-DDE (0.60 and 0.66, respectively). Comparisonof DDT associations in nested models are shown in Table2, in which the best model included o,p�-DDT and p,p�-DDE (model 4, Table 2). Independent of a maternal his-tory of breast cancer, elevated maternal serum o,p�-DDTsignificantly predicted a nearly 4-fold increase in thedaughter’s risk of breast cancer (Table 3). Maternal over-weight in early pregnancy was associated with a lower riskof breast cancer in daughters but with marginal statisticalsignificance. Maternal lipids, age, race, and parity andwhether the daughter was breast-fed did not confoundthese findings and were not significant predictors ofdaughters’ breast cancer. No interactions were statisti-cally significant.

Most cases in this cohort were estrogen receptor posi-tive (83%), progesterone receptor positive (76%), andHER2-negative (74%). In human breast cell lines, DDTactivates HER2, a clinically relevant protein expressed insome breast cancers (35, 36). Therefore, we evaluatedwhether in utero DDT exposure was associated withHER2-positive breast cancers in this cohort of women

Table 1. Maternal Variables by Daughters’ Breast Cancer Status

Maternal Variables Controls (n � 315) Cases (n � 103)

Percentile Percentile

25th 50th 75th 25th 50th 75th

Age, y 22 26 30 23 27 31o,p�-DDT, ng/mL 0.27 0.46 0.78 0.32 0.52 1.06p,p�-DDT, ng/mL 8.38 12.98 18.57 9.47 13.18 20.11p,p�-DDE, ng/mL 29.29 42.81 57.56 30.91 43.13 58.08Cholesterol, mg/dL 182 222 278 188 227 283Triglycerides, mg/dL 139 183 227 136 182 227

Percent n Percent NHistory of breast

cancera4.44 14 20.39 21

Primipara 29.84 94 26.21 27African-American 25.08 79 23.30 24Overweight (BMI �

25 kg/m2)25.08 79 17.48 18

Breast-fed herdaughter

26.03 82 31.07 32

Abbreviation: BMI, body mass index.a P � .0001 for difference between controls and cases.



with available stage at diagnosis (73%) and availableHER2 status (59%).

We found that o,p�-DDT was significantly, positivelyassociated with advanced stage at diagnosis (regional ordistant disease vs local or in situ) and with the occurrenceof HER2-positive tumors, independent of maternal over-weight, history of breast cancer, and p,p�-DDE. Despitesmall sample sizes for these analyses, 22 advanced-stagetumors and 16 HER2-positive tumors, respectively, re-sults were statistically significant. The estimated odds ra-tio (OR) for diagnosis at an advanced stage was 2.2 [95%

confidence interval (CI) 1.1–4.2, P � .02] for a doublingof o,p�-DDT. The estimated OR for a HER2-positive tu-mor was 2.1 (95% CI 1.0–4.8, P � .05) for a doubling ofo,p�-DDT. Levels of o,p�-DDT not only doubled but alsotripled for women in the fourth quartile of the study com-pared with those in the first quartile (as seen in Table 1).The corresponding risk of advanced-stage and HER2-pos-itive breast cancer for these women is more than 4-fold (forlate stage, OR 4.6; 95% CI 1.3–16.5 for the fourth quartileof o,p�-DDT vs the first quartile; for HER2 positive, OR4.6, 95% CI 1.1–19.7). These results suggest a strong ef-fect of in utero o,p�-DDT on breast cancer stage, andHER2 status in this population, and the relevance of thesefindings is discussed below.

Discussion

Strengths

Exposure timingHuman and animal evidence establish the existence of

developmental windows when the breast is more vulner-able to xenoestrogens, such as DDT (9). One of these win-dows is in utero. The present study is the first to quantifyexposure to DDT in utero and link it to subsequent breastcancer risk.

Quantifying exposureDDT was introduced in the general population in the

United States in 1945 and was most heavily used world-wide in the late 1950’s and 1960’s (37). The CHDS en-rolled pregnancies during 1959–1967, which, by coinci-dence, covered the years of highest DDT exposure (26,

Table 2. DDT Results for Nested Models

o,p�-DDT p,p�-DDT p,p�-DDE

OR OR OR

Univariate modelsModel 1, o,p�-DDT

Quartile 2 1.8 – –Quartile 3 1.6 – –Quartile 4 2.8a – –P trend 0.053 – –

Model 2, p,p�-DDTQuartile 2 – 1.9 –Quartile 3 – 1.5 –Quartile 4 – 2.2b –P trend – 0.074 –

Model 3, p,p�-DDEQuartile 2 – – 1.3Quartile 3 – – 1.1Quartile 4 – – 1.3P trend – – NS

Model 4, o,p�-DDT plus p,p�-DDEQuartile 2 2.0 – 1.0Quartile 3 1.8 – 0.7Quartile 4 3.7c – 0.7P trend 0.048 – NS

Model 5, p,p�-DDT plus p,p�-DDEQuartile 2 – 2.0 1.1Quartile 3 – 1.7 0.8Quartile 4 – 2.9d 0.8P trend – 0.037 NS

Model 6, o,p�-DDT plus p,p�-DDT plus p,p�-DDEQuartile 2 1.9 1.7 1.0Quartile 3 1.7 1.2 0.7Quartile 4 3.5e 1.4 0.6P trend NS NS NS

Abbreviation: NS, not significant. All models are adjusted for maternalcholesterol and triglycerides, maternal overweight in early pregnancy,and maternal history of breast cancer. P trend is based on continuouslog-transformed DDTs. Model 4 is the best model because deletion ofp,p�-DDT (model 4 vs model 5) does not impact other associations, butdeletion of p,p�-DDE (model 1 vs model 4) decreases the pointestimate for o,p�-DDT. Although p,p�-DDE is not itself significant, it isinversely associated with daughters’ breast cancer while beingpositively correlated with o,p�-DDT. NS, P � .15.a P � .007.b P � .058 .c P � .004 .d P � .054 .e P � .019.

Table 3. Maternal Predictors of Daughters’ BreastCancer

OR 95% CIP

Value

History of breast cancer ( yesvs no)

6.4 2.8–14.3

�.0001

Overweight in early pregnancy( yes vs no)

0.6 0.3–1.1 .077

o,p�-DDT (reference category is quartile 1)Quartile 2 2.0 0.9–

4.3.083

Quartile 3 1.8 0.8–4.0

.160

Quartile 4 3.7 1.5–9.0 .004P trend 0.048

Quartile cut points are given in Table 1. This table is based on a singlemodel adjusted for variables shown and also adjusted for the maternalserum p,p�-DDE, total cholesterol, and total triglycerides, which werenot significant predictors. Test for trend was based on log-transformedo,p�-DDT entered as a continuous variable instead of quartile variables.



38). Consistent with these data, the CHDS maternal serumsamples, which were collected during the peak years ofDDT use in the United States, show the highest levels ofDDT compared with other studies of breast cancer inwhich samples were collected in later decades (11, 13).Thus, the present study uses unique historic samples toquantify typical in utero exposure when DDT use was atits peak. Our laboratory methods were able to quantifythree DDT target compounds in all samples, including thelower concentration o,p�-DDT, a 15%–20% contami-nant of technical DDT. This strength is due to state-of-the-art laboratory methods, which optimized the detec-tion of all compounds, but is also due to collection ofserum samples in the 1960’s during a time period whenthere was high use of technical DDT.

Relevance to countries in which DDT is now bannedDDT was banned in the 1970’s in the United States and

western Europe (39). However, the women exposed mostheavily while in utero during the 1960’s are currentlyreaching the age of heightened breast cancer risk. Recentcases of breast cancer in daughters (F1) in the CHDS co-hort represent the leading edge of birth cohorts heavilyexposed to DDT when in utero. Thus, the findings of thispresent study are relevant to breast cancer, even in coun-tries in which DDT is not currently used. In addition, DDTremains a global environmental contaminant due to itsenvironmental persistence and semivolatility (25).

Relevance to countries in which DDT is still usedIn those countries that continue to use DDT to control

malaria, human exposure remains high (40). Thus, thefindings of this study are relevant to current populationsin which high in utero exposure is certainly occurring,such as in South Africa (23). The impact of DDT use onunborn generations has been recently raised as an ethicalconsideration (41). Our findings are relevant to thisdebate.

PlausibilityDDTs have been studied as possible endocrine disrup-

tors on the basis of observed deleterious reproductive ef-fects in wildlife (39, 42) and based on demonstrated en-docrine-active effects including estrogen activity,particularly for o,p�-DDT (43, 44). Remarkably, indepen-dent of estrogen, there is likely a biological basis for theputative association of in utero DDT and HER2-positivecancers (36, 45, 46). For example, low-dose o,p�-DDT (1nM) enhanced the tyrosine kinase activity of HER2 inhuman MCF-7 breast cancer cells irrespective of tamox-ifen exposure or estrogen depletion of culture media (36,46). o,p�-DDT also gave rise to increased MCF-7 foci (ab-

normal concentric piling up of cells in postconfluent cul-tures) (46). The effects of o,p�-DDT on tyrosine kinaseactivity of HER2 and MCF7 foci formation were blockedby a mononuclear antibody specific to HER2. These ex-perimental results are consistent with the hypothesis thispaper supports that o,p�-DDT can cause human mam-mary tumor formation that depends on the activation ofHER2 (36, 46). Although this hypothesized effect of inutero DDT exposure on mammary cancer has not yet beentested experimentally in vivo, when exposure to its me-tabolite p,p�-DDE was initiated at weaning, the latency ofHER2-positive mouse mammary tumors was shortened(47). Our nested pilot analysis also suggested that highexposure was significantly associated with advancedstage. Although no in vivo studies have evaluated this, arecent study of human breast cancer cell lines suggestedo,p�-DDT caused estrogen-dependent invasion (48). Pri-oritizing the acquisition of tumor blocks and their immu-nohistochemical analysis of estrogen receptor and HER2in the ongoing CHDS and in parallel experimental modelswill likely aid in resolving which receptor is the mecha-nistic target of in utero DDT on mammary carcinogenesis.

DES is the most well-studied perinatal xenoestrogenexposure in humans and is known to be associated withincreased risk of breast cancer in both F0 (exposed in preg-nancy) (49) and F1 (exposed in utero) (3). Similar to DES,we found that maternal serum p,p�-DDT was associatedwith an increased risk of breast cancer in CHDS mothers(F0) (11). We used birth year as a proxy for earliest age atDDT exposure and found the strongest association wasobserved in mothers who were initially exposed to DDTbefore the age of 4 years (11). The present study providesa direct, quantitative measure of exposure in utero fordaughters (F1) in the CHDS and also finds an associationbetween in utero DDT exposure and breast cancer.

Limitations

Outcome windowThe present study investigates breast cancer diagnosed

before age 52 years. Thus, these results do not addressDDT associations with breast cancer diagnosed at a laterage. One prior study of dioxin exposure to girls andwomen after a chemical explosion in Seveso, Italy, re-ported a significant association for breast cancers diag-nosed within the first 20 years, which then declined overthe subsequent 10 years of follow-up (50). Continuingfollow-up in our cohort will be required to determinewhether in utero DDT associations with breast cancer areobserved for cases diagnosed in the future.



Exposure windowWhereas we have measured exposure directly relevant

to fetal life, we cannot rule out a contribution of postnatalexposure. We did not observe a contribution or synergywith breast-feeding, even though this is a major maternalroute of DDT exposure to offspring. However, this neg-ative association may be partly explained by the low fre-quency of breast-feeding in the CHDS and the relativelysmall sample size.

Unmeasured confoundersWe cannot rule out a contribution of other exposures

that are correlated to DDT, including other unmeasuredDDT metabolites. However, we were able to account forthe DDTs that are present in the highest concentration inwomen.

Small sampleThis study investigates the first cases observed in CHDS

daughters. Although the sample size was adequate to ob-serve a sizable association with in utero DDT, we are un-likely to have had the power to observe smaller associa-tions with other risk factors or synergy among variables.To date, incomplete data on tumor pathology limits theinterpretation of the correlation between DDT and tumorswith more aggressive features.

SummaryWe observed a sizable, statistically significant associa-

tion between in utero DDT exposure and risk of breastcancer in young women and a possible association withmore aggressive tumors. These findings are the first everreported for a prospective observation of a large preg-nancy cohort. Experimental studies are essential to con-firm findings and discover causal mechanisms. If con-firmed, these findings could lead to discovery ofbiomarkers and interventions for DDT-associated breastcancer. Our findings are relevant to the international de-bate on the costs and benefits of DDT use for malariacontrol.

Acknowledgments

We acknowledge the late Jacob Yerushalmy, who founded theChild Health and Development Studies cohort; the late Barbaravan den Berg, the second Director of the Child Health and De-velopment Studies; and her colleague, Roberta Christianson,who ensured its quality and longevity.

Address all correspondence and requests for reprints to: Bar-bara A. Cohn, PhD, Child Health and Development Studies,1683 Shattuck Avenue, Suite B, Berkeley, CA 94709. E-mail:[email protected].

The point of view and conclusions expressed in this paper arethose of the authors and do not necessarily represent the officialposition or policies of the funding agencies.

The ideas and opinions expressed herein are those of the au-thor(s) and endorsement by the State of California, Departmentof Public Health the National Cancer Institute, and the Centersfor Disease Control and Prevention or their contractors and sub-contractors or any of the funders of this research is not intendednor should be inferred.

This work was supported by funding from the CaliforniaBreast Cancer Research Program through the Special ResearchInitiative under Grant 15ZB-0186; National Institute of Envi-ronmental Health Sciences Grant R00 ES019919; Eunice Ken-nedy Shriver National Institute of Child Health and Develop-ment, National Institutes of Health, Department of Health andHuman Services Contract HHSN275201100020C. The collec-tion of cancer incidence data used in this study was supported bythe California Department of Public Health as part of the state-wide cancer reporting program mandated by California Healthand Safety Code Section 103885; the National Cancer Institute’sSurveillance, Epidemiology, and End Results Program underContract HHSN261201000140C (awarded to the Cancer Pre-vention Institute of California), ContractHHSN261201000035C (awarded to the University of SouthernCalifornia), and Contract HHSN261201000034C (awarded tothe Public Health Institute); and the Centers for Disease Controland Prevention’s National Program of Cancer Registries, underAgreement U58DP003862–01 (awarded to the California De-partment of Public Health).

Disclosure Summary: The authors have nothing to disclose.

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E-mail this pageMore press releasesFor Immediate Release, June 23, 2015

Contact Brett Hartl, (202) 817-8121, [email protected]

Settlement: EPA to Analyze Impacts of World's Two Most Widely Used Pesticides on1,500 Endangered Species

Historic Settlement Means Harms of Atrazine, Roundup Will Be Assessed

WASHINGTON— The Environmental Protection Agency will analyze the impacts of atrazine and glyphosate — the two most commonly usedpesticides in the United States — on 1,500 endangered plants and animals in the United States under the terms of a settlement reached todaywith the Center for Biological Diversity. The EPA will also analyze the impacts of propazine and simazine, two pesticides that are chemicallysimilar to atrazine. It has committed to completing the assessments by June 2020.

“This settlement is the first step to reining in the widespread use of dangerous pesticides that are harming both wildlife and people,” said BrettHartl, endangered species policy director at the Center for Biological Diversity. “Atrazine, for instance, chemically castrates frogs even in tinydoses, is an endocrine disruptor, and likely causes birth defects in people. The EPA should have banned this years ago.”

Up to 80 million pounds of atrazine are used in the United States each year. In addition to causing severe harm to endangered species, atrazineexposure may be linked to increased risks of thyroid cancer, reproductive harm and birth defects in people. A recent study showed that childrenwhose mothers were exposed to atrazine had an increased risk of birth defects. Atrazine is the second most commonly used pesticide afterglyphosate, more commonly known as Monsanto’s Roundup.

“This settlement will finally force the EPA to consider the impacts of glyphosate — widely known as Roundup — which is the most commonlyused pesticide in the United States, on endangered species nationwide,” said Hartl. “With more than 300 million pounds of this stuff beingdumped on our landscape each year, it’s hard to even fathom the damage it’s doing.”

Glyphosate has also been linked to the decline of many wildlife species, including the monarch butterfly. The EPA has never completed anyendangered species assessments of glyphosate at any point over the lifetime of this chemical on the market. The agency last evaluated thegeneral ecological impacts of glyphosate in 1993, when approximately 10 million pounds were applied annually. The increase in use within theUnited States has come with the widespread adoption of herbicide-tolerant, genetically engineered crops such as corn and soy. The WorldHealth Organization recently declared glyphosate a probable human carcinogen.

The EPA has, for decades, continued to register and allow the use of pesticides without considering their impacts to endangered species,despite the legal requirement for them to do so and the well-documented risks of pesticides to thousands of imperiled species. A series oflawsuits by the Center has forced the agency to consult on the impacts of scores of pesticides on some endangered species, primarily inCalifornia, and resulted in temporary restrictions on pesticide use in sensitive habitats.

Last year the Center entered a nationwide settlement with the U.S. Fish and Wildlife Service requiring the agency to analyze impacts onendangered species across the country from five dangerous pesticides — carbaryl, chlorpyrifos, diazinon, malathion and methomyl — that havebeen found to be toxic to wildlife and may pose a health risk to humans. Today’s settlement follows a similar framework and will require the EPAto begin the consultation process on these chemicals.

The Center for Biological Diversity is a national, nonprofit conservation organization with more than 900,000 members and online activistsdedicated to the protection of endangered species and wild places.

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Health | Tue Jun 23, 2015 5:51am EDT

LONDON | BY KATE KELLAND

The insecticide lindane, once widely used in agriculture and to treat human lice andscabies, causes cancer and has been specifically linked to non-Hodgkin lymphoma, theWorld Health Organization said on Tuesday.

The WHO's International Agency for Research on Cancer (IARC) also said that DDT, ordichlorodiphenyltrichloroethane, probably causes cancer, with scientific evidence linking itto non-Hodgkin lymphoma (NHL), testicular cancer and liver cancer.

In a review of various agricultural chemicals, IARC's specialist panel said it had decided toclassify lindane as "carcinogenic to humans" in its Group 1 category, DDT as "probablycarcinogenic to humans" in its Group 2A class, and the herbicide 2,4-D as "possiblycarcinogenic to humans" in its Group 2B.

It said epidemiological studies did not find strong or consistent increases in risk of NHL orother cancers from 2,4-D exposure, but there was strong evidence it induces oxidativestress, a process that can damage cells in the body, and moderate evidence it cansuppress the immune system.

Lindane, which since 2009 has been banned or restricted in most countries under theStockholm Convention on Persistent Organic Pollutants, was previously used extensivelyfor insect control in agriculture. An exemption to the ban allows it to be used as asecond-line treatment for lice and scabies.

IARC said high exposures to lindane have previously been reported among agriculturalworkers and pesticide applicators.

"Large epidemiological studies of agricultural exposures in the United States and Canadashowed a 60 percent increased risk of non-Hodgkin lymphoma in those exposed tolindane," it said.

DDT was introduced for the control of insect-borne diseases during World War Two andwas later applied widely to eradicate malaria and in agriculture.

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Although most uses of it were banned from the 1970s, IARC cautioned that DDT and itsbreakdown products are "highly persistent and can be found in the environment and inanimal and human tissues throughout the world".

"Exposure to DDT still occurs, mainly through diet," it said, adding that DDT is still used,mainly for malaria control in parts of Africa, although under very strict conditions.

Since it was introduced in 1945, 2,4-D has been widely used to control weeds inagriculture, forestry and urban and residential settings.

IARC said occupational exposure to 2,4-D can occur during manufacturing and application,and people in the general population can be exposed through food, water, dust, orresidential application, and during spraying.

(Reporting by Kate Kelland; Editing by Raissa Kasolowsky)

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The city of Oslo The city of Oslo now has what it's calling a bee highwaynow has what it's calling a bee highway — a path of flowering plants designed to keep bees well-fed as they pass through the urban area. — a path of flowering plants designed to keep bees well-fed as they pass through the urban area.

Supporters hope that initiatives like this one can help protect bees — one third of Norway's native bee species are now endangered — and by extensionSupporters hope that initiatives like this one can help protect bees — one third of Norway's native bee species are now endangered — and by extension

protect the crops that rely on bees for pollination.protect the crops that rely on bees for pollination.

The idea is pretty simple: The Oslo Garden Society has placed flowerpots full of bee-friendly plants on roofs and balconies throughout the city, creating aThe idea is pretty simple: The Oslo Garden Society has placed flowerpots full of bee-friendly plants on roofs and balconies throughout the city, creating a

route for bees to travel through without starving. route for bees to travel through without starving. A Web site shows localsA Web site shows locals where more flower coverage is needed and encourages them to plant more. where more flower coverage is needed and encourages them to plant more.

[[Graphic: We all get stung by bee coloGraphic: We all get stung by bee colonyny collapse collapse]]

“The idea is to create a route through the city with enough feeding stations for the bumblebees all the way,” Tonje Waaktaar Gamst of the Oslo Garden“The idea is to create a route through the city with enough feeding stations for the bumblebees all the way,” Tonje Waaktaar Gamst of the Oslo Garden

Society Society told a local paper in Maytold a local paper in May. “Enough food will also help the bumblebees withstand man-made environmental stress better.”. “Enough food will also help the bumblebees withstand man-made environmental stress better.”

Agence France-Presse reportsAgence France-Presse reports that businesses have also joined in, with one accounting firm putting up around $50,000 to cover its terrace in flowering that businesses have also joined in, with one accounting firm putting up around $50,000 to cover its terrace in flowering

plants and enough beehives to house 45,000 bees.plants and enough beehives to house 45,000 bees.

[[Why you shouldn’t freak out about swarming honeybees — and how to save bees from those who doWhy you shouldn’t freak out about swarming honeybees — and how to save bees from those who do]]

The The decline of the pollinating beedecline of the pollinating bee — and the potential causes of that decline, which could include fungi, pests, lack of food and pesticide use — is a subject of — and the potential causes of that decline, which could include fungi, pests, lack of food and pesticide use — is a subject of

much debate. But while the restriction of pesticides like much debate. But while the restriction of pesticides like neonicotinoidsneonicotinoids, which some believe have an adverse effect on honeybees, may not make sense, which some believe have an adverse effect on honeybees, may not make sense

without more evidence, planting flowers is a fix that's hard to argue with.without more evidence, planting flowers is a fix that's hard to argue with.

Besides, Besides, research suggestsresearch suggests that so-called “green spaces” in urban areas — ones with trees, grass, flowers, and animals — are beneficial to human health and that so-called “green spaces” in urban areas — ones with trees, grass, flowers, and animals — are beneficial to human health and

wellness. So planting flowers for transient bees is really a win-win.wellness. So planting flowers for transient bees is really a win-win.

Those outside of Oslo can take advantage of a similar site with a global reach. Those outside of Oslo can take advantage of a similar site with a global reach. The Pollinator PartnershipThe Pollinator Partnership encourages individuals to create bee-friendly encourages individuals to create bee-friendly

environments on their property and add them to an online map.environments on their property and add them to an online map.

Read More:Read More:

Bill Nye explains how climate change works (with emoji, obviously)Bill Nye explains how climate change works (with emoji, obviously)

New studies find that bees actually want to eat the pesticides that hurt themNew studies find that bees actually want to eat the pesticides that hurt them

How the White House plans to help the humble bee maintain its buzzHow the White House plans to help the humble bee maintain its buzz

Norway is creating a ‘bee highway’ to protect pollinators - The Washingt... http://www.washingtonpost.com/news/speaking-of-science/wp/2015/06/...

2 of 2 6/25/2015 4:12 PM

http://www.komonews.com/news/local/Agriculture-department-investigating-Portland-bee-die-off-310356521.html

Agriculture department investigating Portland bee die-off By Associated Press Published: Jun 27, 2015 at 3:31 PM PDT

PORTLAND, Ore. (AP) - The fifth mass bee death in Portland in the past several days has state investigators on the hunt for a cause. The Oregonian reports that dead and dying bumblebees littered the sidewalk in some parts of the city. Oregon Department of Agriculture lead pesticide investigator Mike Odenthal says lab results from the earlier die-offs are expected next week. He says the department is trying to find out whether humans did something to the bees with a pesticide or pollutant or whether there's something strange going on with the linden tree blossoms the pollinators had been feeding on. Every major bee die-off reported to the agriculture department in the past few years has taken place near the trees, which are often sprayed with chemicals to control

Cause unknown in spate of Portland bee die-offsKelly House | The Oregonian/OregonLive By Kelly House | The Oregonian/OregonLive

Email the author | Follow on Twitter

on June 26, 2015 at 5:26 PM

Corinne Fletcher stepped outside her apartment building Friday morning to find a pollinator genocide in the park that serves as her backyard.

Dead and dying bumblebees littered the sidewalk near the Market Street entrance to downtown Portland's Pettygrove Park. The carcasses were

so thick, the Lewis & Clark College law student said, "you had to step carefully to not step on any bees."

The fifth mass bee death in Portland in the past several days has state investigators on the hunt for a cause.

Lab results from the first four die-offs are expected next week, said Mike Odenthal, lead pesticide investigator for the Oregon Department of

Agriculture.

It's too early to say what killed the bees, but all of the die-offs share a similarity: The bees had been feeding on linden tree blossoms.

"We're trying to find out whether this is something humans did to the bees – a pesticide or pollutant or something – or is there something weird

going on with the trees?" Odenthal said.

Every major bee die-off reported to the Oregon Department of Agriculture in the past few years has taken place near the trees, which are often

sprayed with chemicals to control aphids.

"They don't harm the tree, but they secrete a honeydew that's considered a nuisance," said Aimee Code, pesticide program coordinator for the

Xerces Society for Invertebrate Conservation.

A high profile poisoning in 2013 of more than 50,000 bees in a Wilsonville Target superstore parking lot raised public awareness about bee

deaths. A class of insecticides known as neonicotinoids were at fault in the Wilsonville incident and several subsequent Oregon bee die-offs.

The incidents spurred state and local restrictions on the use of neonicotinoids. A statewide ban on the use of four types of neonicotinoids on

linden trees and related species took effect in February. Portland followed suit in April with a ban on the use of all neonicotinoids on city lands.

After reaching out to Portland Parks and the Xerces Society, Fletcher took Code's advice to return to the park and collect bees for state testing.

By the time she returned, she said, "a lot of them were gone."

A worker in one of the adjacent buildings told her bees in the park have been dropping dead daily for more than a month.

Mark Ross, spokesman for Portland Parks & Recreation, said the agency does not spray insecticides at Pettygrove Park.

Most of the dead bees found Friday appeared to be concentrated on the sidewalk just outside the park, where bees were swarming several large

linden trees in full bloom.

There's little chance they died of natural causes, Code said. Mass mortality events aren't part of the bumblebee life cycle.

But it's not certain insecticides or other chemical applications are to blame, either. When stressed, lindens sometimes produce a sugar that can be

dangerous to bees.

If Fletcher collects enough bees to conduct testing, lab analysts will look for substances that could have killed them. If any banned neonicotinoids

show up, investigators will have to ask another question: Were the chemicals applied before or after the state's ban took effect in February?

Neonicotinoids can remain present at levels lethal to bees for months after application on a tree, Odenthal said.

"It's possible we may have had a legal application of a now-banned product before we banned it, that's causing the activity now," he said.

Cause unknown in spate of Portland bee die-offs http://blog.oregonlive.com/environment_impact/print.html?entry=/2015/...

1 of 2 6/29/2015 8:55 AM

What to do if you spot a bee die-off?

Call The Oregon Department of Agriculture, take a photo and ask whether you should collect a sample. As Fletcher experienced in Pettygrove

Park, the bodies are often swept or blown away before state investigators arrive.

Code offers another piece of advice.

"Create a habitat in your hard that is pesticide-free with many options for foraging and food sources for bees," she said.

-- Kelly House

[email protected]

503-221-8178

@Kelly_M_House

© 2015 OregonLive.com. All rights reserved.

Cause unknown in spate of Portland bee die-offs http://blog.oregonlive.com/environment_impact/print.html?entry=/2015/...

2 of 2 6/29/2015 8:55 AM

News-Times Connecticut Post The Advocate Greenwich Time Community W

Pesticides banned on municipal playgrounds in CT - Jonathan Kantrowitz http://blog.ctnews.com/kantrowitz/2015/07/01/pesticides-banned-on-mun...

1 of 6 7/2/2015 2:00 PM

Pesticides banned on municipal playgrounds in CT - Jonathan Kantrowitz http://blog.ctnews.com/kantrowitz/2015/07/01/pesticides-banned-on-mun...

2 of 6 7/2/2015 2:00 PM

Mateusz PerkowskiCapital Press

Published:June 30, 2015 5:22PM

The EPA says it plans to ban the common insecticide chlorpyrifos but may change its mind based on discussions with manufacturers.

The federal government said June 30 that it’s planning to ban chlorpyrifos, a common insecticide, but may change its mind based on consultations with thechemical’s manufacturer.

The U.S. Environmental Protection Agency’s tentative decision to revoke all “tolerances” for residues of the insecticide on crops came in response to a requestfrom environmental groups.

Pesticide Action Network North America and the Natural Resources Defense Council claim that exposure to the chemical causes farmworkers’ children toexperience long-term health problems, among other problems.

The EPA is signaling that it may take action on chlorpyrifos but “there are many opportunities for going astray and failing to protect communities from thischemical,” said Paul Towers, spokesperson for PANNA.

The groups petitioned EPA to prohibit chlorpyrifos based on numerous risks in 2007, but the agency did not take final action on the request, arguing it would taketime to study the issue.

The 9th U.S. Circuit Court of Appeals recently ordered the EPA to make up its mind, which led to the filing of the June 30 report in which the agency said it wouldpropose canceling all chlorpyrifos tolerances by April 2016.

While it was initially inclined to deny the petition in favor of “additional risk mitigation action” to reduce hazards, the EPA is now “less confident” it can achievethat goal without formal regulatory proceedings, the report said.

In some watersheds, potential exposure to the chemical through drinking water and other pathways has prevented the agency from finding “that there is areasonable certainty of no harm to people who would be drinking such water,” the report said.

The EPA noted that threats to agricultural employees may also justify new restrictions on the chemical.

Before proposing the revocation, though, the agency plans to conduct an in-depth assessment to see which watersheds are most vulnerable to chlorpyrifoscontamination.

The EPA also plans to negotiate with the chemical’s manufacturers to potentially revise the pesticide label and avoid hazardous applications of chlorpyrifosrather than have the chemical tolerances revoked.

Towers, of PANNA, said he’s concerned that any changes agreed to by manufacturers will fall short of what’s necessary to protect human health.

“The proof will come months down the road,” he said.

EPA to propose banning chlorpyrifos insecticide - - Capital Press http://www.capitalpress.com/Nation_World/Nation/20150630/epa-to-pro...

1 of 1 7/2/2015 2:02 PM

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California regulations have changed Chlorpyrifos to a "restricted use" pesticide. Applicators will need a permitfrom county agriculture commissioners to use products with Chlorpyrifos in them.Getty Images

New regulations: Chlorpyrifos labeled 'restricted use' inCalifornia effective July 1Farm Press Staff | Western Farm Press

Contact local agriculture commissioner's office for permit requirements

Chlorpyrifos is labeled effective July 1, 2015 as a restricted material in California when itis an ingredient in pesticides for use in the production of an agricultural commodity.

Applicators will need to obtain a restricted materials permit from their county agriculturecommissioner if they wish to purchase, possess or apply affected chlorpyrifos products.

The California Department of Pesticide Regulations (DPR) is currently developing interimpermit condition recommendations, this will be additional mitigation to the instructionsusers of restricted materials must follow.

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The interim permit conditions may include buffer zones near sensitive sites, GMP (goodmanagement practices) to prevent drift or offsite movement into the air and measures toreduce runoff into surface waters.

County agriculture commissioners will be notified by the DPR with a letter of therecommended interim conditions.

A list of products published by DPR includes 31 pesticides that will be affected by the newregulation.

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